Cancer is visualized as a possible end result of an adaptive process to chronic cellular injury. Also, it is postulated that a relationship exists between cytotoxicity and carcinogenesis. Acute hepatotoxicity, manifested by disaggregation of liver polysomes and inhibition of protein synthesis can be observed in the rat following the administration of a large dose of any one of several chemical agents (aflatoxin B1, dimethylnitrosamine, p- dimethylaminoazobenzene and quinoline analogues, ethionine, lasiocarpine, retrosine and tannic acid) which when given for prolonged periods of time in a lesser dosage are carcinogenic. Preliminary experiments with one of these agents, ethionine, suggest that during hepatocarcinogenesis the liver cells adapt and become less sensitive to the acute toxic effects of ethionine. Although disaggregation of liver polysomes may represent a non- specific event during cell injury, the ability of the liver cells to adapt to toxic agents and develop resistance to polysome disaggregation may be specific of carcinogenesis. Such an adaptation would reflect a change in regulatory mechanisms of polysome structure and protein synthesis. Means of exploring the nature of the cellular components involved and the cell populations affected are offered.